Comparative effect of FGF2, synthetic peptides 1-28 N-POMC and ACTH on proliferation in rat adrenal cell primary cultures

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Citações na Scopus
18
Tipo de produção
article
Data de publicação
2011
Título da Revista
ISSN da Revista
Título do Volume
Editora
SPRINGER
Autores
MATTOS, Gabriele E.
AMARANTE-MENDES, Gustavo P.
LOTFI, Claudimara Ferini Pacicco
Citação
CELL AND TISSUE RESEARCH, v.345, n.3, p.343-356, 2011
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
There is evidence that pro-opiomelanocortin (POMC)-derived peptides other than adrenocorticotropic hormone (ACTH) have a role in adrenal cell proliferation. We compared the activity of synthetic rat N-terminal POMC fragment 1-28 with disulfide bridges (N-POMC(w)) and without disulfide bridges (N-POMC(w/o)), with the activity of fibroblast growth factor (FGF2), a widely studied adrenal growth factor, and ACTH, in well-characterized pure cultures of both isolated adrenal Glomerulosa (G) and Fasciculata/Reticularis (F/R) cells. Three days of FGF2-treatment had a proliferative effect similar to serum, and synthetic peptide N-POMC(w) induced proliferation more efficiently than N-POMC(w/o). Moreover, both induced proliferation via the ERK1/2 pathway. In contrast, sustained ACTH treatment decreased proliferation and viability through apoptosis induction, but not necrosis, and independently of PKA and PKC pathways. Further elucidation of 1-28 POMC signal transduction is of interest, and primary cultures of adrenal cells were found to be useful for examining the trophic activity of this peptide.
Palavras-chave
Rat primary adrenal culture, 1-28 N-POMC, ACTH, FGF2, Proliferation, Rat (Sprague Dawley)
Referências
  1. Mattos GE, 2005, MOL CELL ENDOCRINOL, V245, P31, DOI 10.1016/j.mce.2005.10.001
  2. Shepherd SP, 2001, AM J PHYSIOL-CELL PH, V280, pC61
  3. Armelin HA, 1999, BRAZ J MED BIOL RES, V32, P841, DOI 10.1590/S0100-879X1999000700007
  4. BASILE DP, 1994, ENDOCRINOLOGY, V134, P2482, DOI 10.1210/en.134.6.2482
  5. Bicknell AB, 2003, ANN NY ACAD SCI, V994, P118
  6. Boulle N, 2000, ENDOCRINOLOGY, V141, P3127, DOI 10.1210/en.141.9.3127
  7. Carsia RV, 1996, CELL TISSUE RES, V283, P247, DOI 10.1007/s004410050535
  8. Carsia RV, 1997, ENDOCRINE, V7, P377, DOI 10.1007/BF02801333
  9. Chu YT, 2009, TISSUE ENG PT A, V15, P2093, DOI 10.1089/ten.tea.2008.0305
  10. ESTIVARIZ FE, 1982, NATURE, V297, P419, DOI 10.1038/297419a0
  11. Fassnacht M, 2003, J CLIN ENDOCR METAB, V88, P2171, DOI 10.1210/jc.2002-021318
  12. GALLOPAYET N, 1989, J ENDOCRINOL, V120, P409, DOI 10.1677/joe.0.1200409
  13. GOSPODAROWICZ D, 1975, ENDOCRINOLOGY, V97, P102
  14. HORNSBY PJ, 1974, ENDOCRINOLOGY, V95, P1240
  15. HORNSBY PJ, 1973, BIOCHEM BIOPH RES CO, V54, P1554, DOI 10.1016/0006-291X(73)91163-7
  16. HORNSBY PJ, 1977, J CLIN INVEST, V60, P342, DOI 10.1172/JCI108782
  17. Lotfi CFP, 1997, J BIOL CHEM, V272, P29886, DOI 10.1074/jbc.272.47.29886
  18. LOWRY PJ, 1983, NATURE, V306, P70, DOI 10.1038/306070a0
  19. MASUI H, 1971, J BIOL CHEM, V246, P5407
  20. MESIANO S, 1991, P NATL ACAD SCI USA, V88, P5428, DOI 10.1073/pnas.88.12.5428
  21. Otis M, 2005, ENDOCRINOLOGY, V146, P633, DOI 10.1210/en.2004-0935
  22. Otis M, 2007, J ENDOCRINOL, V193, P331, DOI 10.1677/JOE-07-0055
  23. Pepper DJ, 2009, MOL CELL ENDOCRINOL, V300, P77, DOI 10.1016/j.mce.2008.09.021
  24. Mendonça Pedro O R de, 2011, Mol Cell Endocrinol, V336, P156, DOI 10.1016/j.mce.2010.12.012
  25. RAMACHANDRAN J, 1975, P NATL ACAD SCI USA, V72, P113, DOI 10.1073/pnas.72.1.113
  26. RAMIREZZACARIAS JL, 1992, HISTOCHEMISTRY, V97, P493, DOI 10.1007/BF00316069
  27. SCHWEIGERER L, 1987, ENDOCRINOLOGY, V120, P796
  28. SIMONIAN MH, 1981, ENDOCRINOLOGY, V108, P1769
  29. Torres TEP, 2010, CELL TISSUE RES, V341, P239, DOI 10.1007/s00441-010-0998-0